雷火灸治疗高脂饮食诱导的睑板腺功能障碍的机制。
Mechanism of Thunder-Fire Moxibustion in the Treatment of Meibomian Gland Dysfunction Induced by High-Fat Diet.
出版信息
Adv Mind Body Med. 2024 Summer;38(3):28-35.
OBJECTIVE
An investigation into whether Thunder-Fire Moxibustion improves Meibomian Gland Dysfunction by activating peroxisome proliferator-activated receptor gamma (PPARγ)-related signaling pathway.
METHODS
C57BL/6 mice were randomly divided into a Control Group (CG), model group (MG), Experimental Group (EG), Treatment Group (TG), and GW9662 (GW), with 10 mice in each group. The obstruction of the meibomian gland opening, tear film rupture time, and corneal fluorescein sodium staining were observed. The morphology of the meibomian gland was observed by HE staining. Observations of oil red staining were made on the meibomian gland to determine its oil content. The expression levels of PPARγ, NF-κB p65, Phospho-NF-κB p65 (p-NF-κB), and IL-6 in the meibomian gland were detected by Western blot. The expression of PPARγ, NF-κB p65, p-NF-κB p65, and IL-6 in the meibomian gland was examined by immunofluorescence staining.
RESULTS
The results showed that compared to the Control Group, the Model Group mice exhibited an increased Meibomian Gland Orifices Score (MGOS) (P < .01), an increased MG corneal staining (P < .01), a shorter tear film break-up time (P < .01), eyelid atrophy, disordered arrangement of meibomian gland cells, the presence of a large number of immature adipocytes, varying degrees of cellular inflammation and infiltration, a significant reduction in meibomian gland tissue lipids, decreased expressions of MGPPARγ and NF-κB (P < .01), and elevated expressions of phosphorylated NF-κB and IL-6 (P < .01). However, Western medicine, antagonists, and thunder-fire moxibustion were all able to reverse these phenomena observed in the Model Group mice (P < .01), with thunder-fire moxibustion exhibiting the most significant effect (P < .01).
CONCLUSION
The thunder-fire moxibustion can induce the differentiation of meibomian gland cells, thereby improving the inflammation response.
目的
探究雷火灸是否通过激活过氧化物酶体增殖物激活受体γ（PPARγ）相关信号通路来改善睑板腺功能障碍。
方法
将 C57BL/6 小鼠随机分为对照组（CG）、模型组（MG）、实验组（EG）、治疗组（TG）和 GW9662 组（GW），每组 10 只。观察泪膜破裂时间、角膜荧光素钠染色、睑板腺开口阻塞情况，HE 染色观察睑板腺形态，油红染色观察睑板腺油脂含量，Western blot 检测 PPARγ、NF-κB p65、磷酸化 NF-κB p65（p-NF-κB）、IL-6 在睑板腺中的表达，免疫荧光染色检测 PPARγ、NF-κB p65、p-NF-κB p65、IL-6 在睑板腺中的表达。
结果
与对照组比较，模型组小鼠睑板腺开口评分（MGOS）增高（P<0.01），MG 角膜染色评分增高（P<0.01），泪膜破裂时间缩短（P<0.01），出现上睑皮肤萎缩、睑板腺细胞排列紊乱、大量不成熟脂肪细胞堆积、不同程度的细胞炎症浸润，睑板腺组织脂质减少，MGPPARγ、NF-κB 表达降低（P<0.01），p-NF-κB、IL-6 表达升高（P<0.01）；西药、拮抗剂及雷火灸均能逆转模型组上述变化（P<0.01），且雷火灸作用最明显（P<0.01）。
结论
雷火灸可诱导睑板腺细胞分化，改善炎症反应。
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